Toll-like receptor 5-mediated IL-17C expression in intestinal epithelial cells enhances epithelial host defense against F4+ ETEC infection

  • Vet Res. 2019 Jun 20;50(1):48. doi: 10.1186/s13567-019-0665-8.
Yu Luo  1 ,  Jia Xu  2 ,  Chaoying Zhang  2 ,  Chunyan Jiang  2 ,  Yanfeng Ma  2 ,  Haijian He  2 ,  Yuan Wu  2 ,  Bert Devriendt  3 ,  Eric Cox  3 ,  Hongbin Zhang  2
Affiliations
  • 1. Animal Medical Testing Center, Department of Animal Production, Faculty of Agricultural & Biological Engineering, Jinhua Polytechnic, Jinhua, China. [email protected].
  • 2. Animal Medical Testing Center, Department of Animal Production, Faculty of Agricultural & Biological Engineering, Jinhua Polytechnic, Jinhua, China.
  • 3. Laboratory of Immunology, Faculty of Veterinary Medicine, Ghent University, Ghent, Belgium.
PMID: 31221216 DOI: 10.1186/s13567-019-0665-8
Abstract

Enterotoxigenic Escherichia coli (ETEC) are an important cause of post-weaning diarrhea (PWD) in piglets. The IL-17 cytokine family is well known to play important roles in the host defense against Bacterial infections at the mucosa. Previously, we reported the potential role of IL-17A in clearing an ETEC Infection in piglets. IL-17C, another member of the IL-17 family, is highly expressed in the intestinal epithelium, however, its role during an ETEC Infection is still unclear. In this study, we demonstrate that F4+ ETEC induce IL-17C mRNA and protein expression in intestinal tissues as well as in porcine intestinal epithelial cells (IPEC-J2). This IL-17C production is largely dependent on TLR5 signaling in IPEC-J2 cells. Both F4+ ETEC Infection and exogenous IL-17C increased the expression of antimicrobial peptides and tight junction proteins, such as porcine beta-defensin (pBD)-2, claudin-1, claudin-2 and occludin in IPEC-J2 cells. Taken together, our data demonstrate that TLR5-mediated IL-17C expression in intestinal epithelial cells enhances mucosal host defense responses in a unique autocrine/paracrine manner in the intestinal epithelium against ETEC Infection.

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